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兔门静脉对组胺的反应。

Responses of rabbit portal vein to histamine.

作者信息

Cook D A, Macleod K M

出版信息

Br J Pharmacol. 1978 Feb;62(2):165-70. doi: 10.1111/j.1476-5381.1978.tb08441.x.

Abstract

1 Histamine produced a dose-dependent contraction of the isolated portal vein of the rabbit. This contraction was not antagonized by atropine, methysergide, indomethacin, cocaine or 6-hydroxy-dopamine, nor by pretreatment of the rabbit with reserpine. 2 The response to histamine was blocked by H1-receptor antagonists only when the blocking agent was used in very high concentrations, and was not antagonized by the H2-receptor blocking agent, metiamide, H1-receptor antagonists did not block the effects of 5-hydroxytryptamine. 3 The contractions elicited by histamine, 5-hydroxytryptamine and noradrenaline were blocked by phentolamine. 4 Desensitization to high doses of 5-hydroxytryptamine caused a concomitant depression in the response to histamine but not to noradrenaline or acetylcholine. 5 The results suggest that the contractions of rabbit portal vein elicited by histamine are not mediated by receptors of the H1- or the H2-type, but may involve an action of histamine at a receptor which is also involved in the action of 5-hydroxytryptamine.

摘要
  1. 组胺可使兔离体门静脉产生剂量依赖性收缩。这种收缩不受阿托品、麦角新碱、吲哚美辛、可卡因或6-羟基多巴胺的拮抗,兔经利血平预处理后也不受影响。

  2. 仅当H1受体拮抗剂以非常高的浓度使用时,对组胺的反应才会被阻断,且不受H2受体阻断剂甲硫米特的拮抗,H1受体拮抗剂不阻断5-羟色胺的作用。

  3. 组胺、5-羟色胺和去甲肾上腺素引起的收缩可被酚妥拉明阻断。

  4. 对高剂量5-羟色胺脱敏会导致对组胺的反应同时降低,但对去甲肾上腺素或乙酰胆碱的反应无此影响。

  5. 结果表明,组胺引起的兔门静脉收缩不是由H1型或H2型受体介导的,而是可能涉及组胺作用于一种也参与5-羟色胺作用的受体。

相似文献

1
Responses of rabbit portal vein to histamine.兔门静脉对组胺的反应。
Br J Pharmacol. 1978 Feb;62(2):165-70. doi: 10.1111/j.1476-5381.1978.tb08441.x.
6
Effects of histamine on the human penis muscle in vitro.
Eur J Pharmacol. 1977 Oct 1;45(3):261-5. doi: 10.1016/0014-2999(77)90008-5.

引用本文的文献

本文引用的文献

1
THE PHARMACOLOGY OF ISOLATED VEINS.离体静脉的药理学
Br J Pharmacol Chemother. 1965 Jun;24(3):742-51. doi: 10.1111/j.1476-5381.1965.tb01630.x.
7
Receptors mediating some actions of histamine.介导组胺某些作用的受体。
Br J Pharmacol Chemother. 1966 Aug;27(2):427-39. doi: 10.1111/j.1476-5381.1966.tb01674.x.

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